Generation of somatic chimeras using genetically-reprogrammed rabbits induced pluripotent stem cells [KEPc]
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PROVIDER: PRJNA1053255 | ENA |
REPOSITORIES: ENA
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Project description:Generation of somatic chimeras using genetically-reprogrammed rabbits induced pluripotent stem cells
| PRJNA1053304 | ENA
Project description:Generation of somatic chimeras using genetically-reprogrammed rabbits induced pluripotent stem cells [KEPi]
| PRJNA1053309 | ENA
Project description:Little is known about the molecular underpinnings of pluripotent stem cells (PSCs)’ ability to colonize preimplantation embryo epiblast to generate chimeras. Using rabbit PSCs as a model system, we conducted unbiased screening of a cDNA library encoding a panel of 36 pluripotency factors. From this, we identified KLF2, ERAS and PRMT6 whose overexpression endows the ability to self-renew in a KOSR/FGF2-free culture medium supplemented with LIF, activin A, PKC and WNT inhibitors. The reprogrammed cells acquired transcriptomic and epigenetic features of naïve pluripotency, including the reactivation of the 2nd X-chromosome. Leveraging on these PSC lines, we determined the transcriptomic signature of embryonic colonization-competence, demonstrating transcriptional repression of genes involved in MAPK, WNT, HIPPO, and EPH signaling pathways, and activation of genes involved in amino-acid metabolism, NF-kB signaling, and p53 pathway. Remarkably, these reprogrammed cells acquired the ability to produce chimeric embryos and fetuses with high contribution from PSCs in all major organs.
2024-12-03 | GSE250287 | GEO
Project description:Little is known about the molecular underpinnings of pluripotent stem cells (PSCs)’ ability to colonize preimplantation embryo epiblast to generate chimeras. Using rabbit PSCs as a model system, we conducted unbiased screening of a cDNA library encoding a panel of 36 pluripotency factors. From this, we identified KLF2, ERAS and PRMT6 whose overexpression endows the ability to self-renew in a KOSR/FGF2-free culture medium supplemented with LIF, activin A, PKC and WNT inhibitors. The reprogrammed cells acquired transcriptomic and epigenetic features of naïve pluripotency, including the reactivation of the 2nd X-chromosome. Leveraging on these PSC lines, we determined the transcriptomic signature of embryonic colonization-competence, demonstrating transcriptional repression of genes involved in MAPK, WNT, HIPPO, and EPH signaling pathways, and activation of genes involved in amino-acid metabolism, NF-kB signaling, and p53 pathway. Remarkably, these reprogrammed cells acquired the ability to produce chimeric embryos and fetuses with high contribution from PSCs in all major organs.
2024-12-03 | GSE250261 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-12-03 | GSE250288 | GEO
Project description:In the murine system, Oct4, Sox2, c-Myc and Klf4 are sufficient to convert fibroblasts to induced pluripotent stem (iPS) cells that exhibit many characteristics of embryonic stem (ES) cells. Herein, we show that the orphan nuclear receptor Esrrb works in conjunction with Oct4 and Sox2 to mediate reprogramming of mouse embryonic fibroblasts (MEFs) to iPS cells. Esrrb reprogrammed cells share similar expression and epigenetic signatures as ES cells. These cells are also pluripotent and can differentiate in vitro and in vivo into the three major embryonic cell lineages. Furthermore, these cells contribute to mouse chimeras and are germline transmissible. In ES cells, Esrrb targets many genes involved in selfrenewal and pluripotency. This suggests that Esrrb may mediate reprogramming through the up-regulation of ES cell-specific genes. Our findings also indicate that it is possible to reprogram MEFs without exogenous Klf transcription factors and link a nuclear receptor to somatic cell reprogramming. We used microarrays to detail the global programme of gene expression of ES cells, Esrrb reprogrammed iPS cell lines and MEFs. Keywords: comparative
2009-01-15 | GSE13211 | GEO
Project description:Creating spontaneous yet genetically tractable human tumors from normal cells presents a fundamental challenge. Retroviruses and transposons have been separately used as somatic cell insertional mutagens to identify cancer drivers in model organisms. Here we combined these mutagenic elements to enable cancer gene discovery starting with normal human cells. Lentivirus was used to seed gain- and loss-of-function gene disruption elements which were further deployed by Sleeping Beauty transposons throughout the genome of human bone explant mesenchymal cells. De novo tumors rapidly generated in this context were high-grade sarcomas corresponding to the spectrum of myxofibrosarcoma and undifferentiated pleomorphic sarcoma, aggressive neoplasms with a predilection for older adults. Tumor insertion sites were genome-wide and enriched in regions of recurrent somatic copy number alteration found in multiple cancers, with a bias towards those of sarcomas. Novel driver genes which sustain somatic alterations in cancer patients were pinpointed. We identify the gene HDLBP, which codes for the RNA binding protein vigilin, as a candidate tumor suppressor deleted at 2q37.3 in greater than one in ten tumors across multiple tissues of origin. Hybrid viral-transposon systems will accelerate the functional annotation of cancer genomes by enabling insertional mutagenesis screens in higher eukaryotes that are not amenable to germline transgenesis.
2014-07-25 | GSE59720 | GEO
Project description:NANOG is required for the long-term establishment of avian somatic reprogrammed cells
| PRJNA432454 | ENA
Project description:Creating spontaneous yet genetically tractable human tumors from normal cells presents a fundamental challenge. Retroviruses and transposons have been separately used as somatic cell insertional mutagens to identify cancer drivers in model organisms. Here we combined these mutagenic elements to enable cancer gene discovery starting with normal human cells. Lentivirus was used to seed gain- and loss-of-function gene disruption elements which were further deployed by Sleeping Beauty transposons throughout the genome of human bone explant mesenchymal cells. De novo tumors rapidly generated in this context were high-grade sarcomas corresponding to the spectrum of myxofibrosarcoma and undifferentiated pleomorphic sarcoma, aggressive neoplasms with a predilection for older adults. Tumor insertion sites were genome-wide and enriched in regions of recurrent somatic copy number alteration found in multiple cancers, with a bias towards those of sarcomas. Novel driver genes which sustain somatic alterations in cancer patients were pinpointed. We identify the gene HDLBP, which codes for the RNA binding protein vigilin, as a candidate tumor suppressor deleted at 2q37.3 in greater than one in ten tumors across multiple tissues of origin. Hybrid viral-transposon systems will accelerate the functional annotation of cancer genomes by enabling insertional mutagenesis screens in higher eukaryotes that are not amenable to germline transgenesis. Lentivirus was used to seed gain- and loss-of-function gene disruption elements which were further deployed by Sleeping Beauty (SB) transposons throughout the genome of human bone explant mesenchymal cells. Genomic locations of LV (lentiviral backbone) and SB insertion sites were mapped by a pooled strategy utilizing linear amplification mediated PCR (LAM-PCR), followed by Illumina next generation sequencing of the product pool.
2014-07-25 | E-GEOD-59720 | biostudies-arrayexpress
Project description:Amami rabbits fecal metagenome
| PRJNA1026798 | ENA